I am really tired of hearing "No Link".
Evidence of Mitochondrial Dysfunction in Autism and Implications for Treatment
Daniel A. Rossignol, J. Jeffrey Bradstreet
International Child Development Resource Center, 3800 W. Eau Gallie Blvd., Suite 105,
Melbourne, FL 32934
Abstract: Classical mitochondrial diseases occur in a subset of individuals with autism and are usually caused by genetic anomalies or mitochondrial respiratory pathway deficits. However, in many cases of autism, there is evidence of mitochondrial dysfunction (MtD) without the classic features associated with mitochondrial disease. MtD appears to be more common in autism and presents with less severe signs and symptoms. It is not associated with discernible mitochondrial pathology in muscle biopsy specimens despite objective evidence of lowered mitochondrial functioning. Exposure to environmental toxins is the likely etiology for MtD in autism. This dysfunction then contributes to a number of diagnostic symptoms and comorbidities observed in autism including: cognitive impairment, language deficits, abnormal energy metabolism, chronic gastrointestinal problems, abnormalities in fatty acid oxidation, and increased oxidative stress. MtD and oxidative stress may also explain the high male to female ratio found in autism due to increased male vulnerability to these dysfunctions.
Biomarkers for mitochondrial dysfunction have been identified, but seem widely under-utilized despite available therapeutic interventions. Nutritional supplementation to decrease oxidative stress along with factors to improve reduced glutathione, as well as hyperbaric oxygen therapy (HBOT) represent supported and rationale approaches. The underlying pathophysiology and autistic symptoms of affected individuals would be expected to either improve or cease worsening once effective treatment for MtD is implemented.
Nutritional supplementation, glutathione, and HBOT represent **supported and rationale approaches**
Three of the major biomed interventions, besides chelation to remove the mercury and other metals to begin with..
These were "supported and rational" approaches in *2008*. If the other 0 cases had been made public, and if they involved mitochondrial disorders, might we have gotten to where we are now in the biomed movement a bit quicker?
One also has to wonder - do mito disorders also have implications in diseases completely separate from autism?
What a mess. But there is still the question of whether mito disorder preceeds autism, or whether it is part of autism. In the end for parents and everyone else, it doesn't matter. But for arguing cases, it does. But was three any previous mito problems in any of these cases, or was it only discovered after autism has been triggered?
Thank you so much for your blog, which I just found by reading from the March 8th article in the New Scientist. I can not for the life of me figure out why people are so blind to the supposed lack of links. I guess I should not be surprised. I for one, am considered crazy because I propose that innocent FDA approved dyes and preservatives have a profoundly negative affect on my daughters health and behavior. It is always my judgment (or parenting) called into question and not the possibility that these dyes are to blame. Thankfully in 2007 some headway was made with a published study in the Lancet. Still, parents must fight on for their children. I will relish the day when more weight is given to the thousands of voices of parents rather than the voices of the few that have vested interests in the products being called into question.
The symptoms of Mitochondrial Myopathy include muscle weakness or exercise intolerance, heart failure or rhythm disturbances, dementia, seizures and other health issues.
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